可溶性TWEAK可预测HIV感染者颈动脉粥样硬化。

Q2 Medicine
HIV Clinical Trials Pub Date : 2017-07-01 Epub Date: 2017-08-22 DOI:10.1080/15284336.2017.1366001
Sahera Dirajlal-Fargo, Abdus Sattar, Manjusha Kulkarni, Nicholas Funderburg, Grace A McComsey
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引用次数: 11

摘要

背景:可溶性肿瘤坏死因子弱诱导凋亡(sTWEAK)被认为是心血管疾病风险的一种新的生物标志物。本研究比较了hiv感染和未感染患者中sTWEAK、sCD163和sCD163/sTWEAK的水平及其与心血管和炎症因子的关系。方法:我们分析的数据来自274名艾滋病毒感染者和59名对照组。艾滋病毒参与者接受稳定的抗逆转录病毒治疗(ART)。Wilcoxon-Mann-Whitney试验用于比较HIV感染参与者与HIV病毒载量之间的标志物结果:总体而言,74%的参与者为男性;59%是非洲裔美国人;中位年龄40岁,CD4 595个细胞/mm3。总体而言,与未感染艾滋病毒的参与者相比,感染艾滋病毒的参与者sTWEAK水平降低,sCD163水平升高(两种标志物的p = 0.0001)。此外,这些生物标志物在hiv感染病毒血症患者和病毒血症患者之间存在显著差异(两种标志物的p≤0.01)。在多变量模型中,病毒血症患者的sTWEAK和sCD163与颈总动脉IMT显著相关(p≤0.05)。在hiv感染的病毒血症参与者中,sTWEAK和sCD163都与IL-6、CD14 + CD16 +单核细胞相关(p≤0.02);此外,sCD163与d -二聚体- (β = -69.5, 0.05), VCAM (β = 72.4, p = 0.05), TNF - RI (β = 91.1, p)相关。结论:hiv感染的参与者表现出全身炎症和单核细胞活化标志物的增加。可溶性CD163和sTWEAK水平与颈动脉内膜-中膜厚度相关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Soluble TWEAK may predict carotid atherosclerosis in treated HIV infection.

Soluble TWEAK may predict carotid atherosclerosis in treated HIV infection.

Background: Soluble Tumor Necrosis Factor Weak Inducer of Apoptosis (sTWEAK) has been proposed as a novel biomarker of cardiovascular disease risk. This study compares levels of sTWEAK, sCD163 and the sCD163/sTWEAK ratio in HIV-infected and uninfected patients and their associations with cardiovascular and inflammatory factors.

Methods: The data for our analysis come from 274 HIV-infected adults and 59 controls. HIV participants were on stable antiretroviral therapy (ART). Wilcoxon-Mann-Whitney tests were used for comparing markers between HIV-infected participants with HIV viral load <50 copies/mL (aviremic group), HIV-infected participants with detectable viremia (HIV-1 RNA ≥50 copies/mL; viremic group) and HIV negative participants. Multivariable quantile regression analyses were used to assess associations of sTWEAK and sCD163 with other markers of inflammation and carotid intima-media thickness (cIMT).

Results: Overall, 74% of participants were male; 59% were African-Americans; median age was 40 years and CD4 595 cells/mm3. Overall, HIV-infected participants had reduced sTWEAK and increased sCD163 levels compared to HIV-uninfected participants (p = 0.0001 for both markers). In addition, these biomarkers were significantly different between HIV-infected viremic and aviremic patients (p ≤ 0.01 for both markers). In multivariable models, sTWEAK and sCD163 in aviremic patients were significantly correlated with common carotid artery IMT (p ≤ 0.05). In HIV-infected aviremic participants, sTWEAK and sCD163 were both associated with IL-6, CD14 + CD16 + monocytes (p ≤ 0.02); additionally, sCD163 was associated with D-dimer- (β = -69.5, 0.05), VCAM (β = 72.4, p = 0.05), TNF RI (β = 91.1, p < 0.01), and TNF RII (β = 87.8, p < 0.01).

Conclusions: HIV-infected participants showed increased systemic inflammatory and monocyte activation markers. Soluble CD163 and sTWEAK levels were associated with carotid intima-media thickness.

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来源期刊
HIV Clinical Trials
HIV Clinical Trials 医学-传染病学
CiteScore
1.76
自引率
0.00%
发文量
0
审稿时长
>12 weeks
期刊介绍: HIV Clinical Trials is devoted exclusively to presenting information on the latest developments in HIV/AIDS clinical research. This journal enables readers to obtain the most up-to-date, innovative research from around the world.
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